Defective iterfering particles modulate rhabdovirus infection of neurons in vitro. This modulation of viral infection is obtained more easily in differentiated neurons. Antibody interaction with vesicular stomatitis virus (VSV) infection neurons activates phagocytic cells, restricts viral maturation sites mostly to postsynaptic area later results in apparent curing of infection. A temperature insensitive revertant of vesicular stomatitis virus causes a lower motor neuron disease in mice with selectve replication in anterior horn cells of the spinal cord in the preclinical stage while neuronal vacuolization is dominant during the disease. In visna infected mouse nerve cells, a slow non-productive infection with progressive fusion of neurons occurs and virus specific proteins are expressed in the virtual absence of viral assembly. A wild measles strain can induce a slow progressive infection of mouse neurons in culture when cells are inoculated early in their differentiation. During antibody dependent lymphocyte cytotoxicity on measles virus infected cells, effector killer cells were studied by rosetting techniques in scanning electron microscopy (EM) and a subpopulation of T cells bearing FC receptors was identified.